Mice lacking NT-3, and its receptor TrkC, exhibit profound deficiencies in CNS glial cells.

Abstract:

:Neurotrophin-3 (NT-3) and its receptor TrkC are known to be important for neuronal survival. More recently, NT-3 has been implicated as playing a role in oligodendrocyte (OL) proliferation and survival in vitro. Examination of NT-3 and TrkC knockout mice revealed a reduction in NT-3-dependent neurons. To date, no study has examined alterations in glial cell populations in these knockout mice. In this report, we demonstrate a decline in OL progenitor cell numbers within the CNS of NT-3 and TrkC knockout mice. We also observed that immature and mature OL-specific markers were attenuated in the NT-3 and TrkC knockout animals. Deficiencies in other CNS glial cells, including astrocytes and ameboid microglia, were also observed. The subventricular zone (SVZ), a highly proliferative region for progenitor glial cells, was reduced in size. Furthermore, a nuclear-specific stain revealed a decline in the numbers of pyknotic nuclei in and around the SVZ of the knockout mice. These data will support an in vivo NT-3-dependent mechanism for the normal development of CNS glial cells.

journal_name

Glia

journal_title

Glia

authors

Kahn MA,Kumar S,Liebl D,Chang R,Parada LF,De Vellis J

subject

Has Abstract

pub_date

1999-04-01 00:00:00

pages

153-65

issue

2

eissn

0894-1491

issn

1098-1136

pii

10.1002/(SICI)1098-1136(199904)26:2<153::AID-GLIA6

journal_volume

26

pub_type

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